Disease relevance of C1QTNF5

• Disease mechanisms in late-onset retinal macular degeneration associated with mutation in C1QTNF5 [1].
• In human and mouse genomes, the MFRP gene lies adjoining to the complement 1q tumor necrosis factor-related protein 5 (CTRP5/C1QTNF5) gene involved in causing retinal degeneration and abnormal lens zonules in human [2].
• Primary fit of the Lord cementless total hip. A geometric study in cadavers [3].
• This idea is called 'the curse of the pharaoh' because of the hypothesis that the death of Lord Carnavon was caused by very long-lived propagules of a highly virulent infectious disease [4].
• We enrolled 98 patients (107 hips) with a mean age of 47 years (SD 8.6) into a prospective study of the Madreporic Lord THR; 34 hips had primary and 73 secondary osteoarthritis [5].

Psychiatry related information on C1QTNF5

• G. Lord and P. E. Levy proposed a variant of control theory that incorporated human information processing principles [6].
• Nine of 17 subjects (53%) met the diagnostic criteria for autistic disorder by the Autism Diagnostic Interview-Revised (ADI-R) algorithm questions [Lord et al., 1993, 1994] [7].
• In that same study, 6 of 13 subjects (46%) met the Autism Diagnostic Interview-Revised (ADI-R) algorithm criteria (Lord et al. [1993] Infant Mental Health 14:234-252; Lord et al. [1994] J Autism Dev Disord 24:659-685) and the Diagnostic and Statistical Manual (APA [1994] DSM-IV) diagnostic criteria for autistic disorder [8].
• This paper reviews the proposals from the Lord Chancellor's Department for new Mental Incapacity law for England and Wales as they may impact on older people with dementia [9].
• "Hear a just cause, O Lord, attend to my cry": organ donation and pastoral care [10].

High impact information on C1QTNF5

• Thirdly, C1QTNF5 is shown to interact with the membrane-type frizzled related protein (MFRP), on the basis of yeast two-hybrid, protein pull-down and co-immunoprecipitation assays and RPE co-localization [1].
• Here, we first show that wild-type C1QTNF5 is secreted, whereas mutant C1QTNF5 is misfolded and retained within the endoplasmic reticulum (ER) [1].
• Mutation in a short-chain collagen gene, CTRP5, results in extracellular deposit formation in late-onset retinal degeneration: a genetic model for age-related macular degeneration [11].
• Here we show that L-ORD is genetically heterogeneous and that a proposed founder mutation in the CTRP5 (C1QTNF5) gene, which encodes a novel short-chain collagen, changes a highly conserved serine to arginine (Ser163Arg) in 7/14 L-ORD families and 0/1000 control individuals [11].
• The nucleotide sequence of the cloned cDNA from one of these classes encodes preproricin and has been presented elsewhere (Lamb, F. I., Roberts, L. M., and Lord, J. M., (1985) Eur. J. Biochem. 148, 265-270) [12].

Biological context of C1QTNF5

• The same CTRP5 missense mutation was identified in all affected individuals [13].
• RESULTS: A significant level of Ctrp5 expression was detected in the adult mouse in the ciliary body (CB) and RPE, and expression started at a very early stage of embryogenesis [14].
• We found reduced levels of genetic diversity compared with tropical reefs (2.75 versus 4 alleles/locus), which supports earlier findings that Lord Howe Island is an isolated reef system [15].
• Sex differences in autism have been described in both singleton and multiplex families [Lord et al., 1982; Volkmar et al., 1993; McLennan et al., 1993; Lord, 1992]: Boys outnumber girls by 3 or 4 to 1, and so a sex-linked mode of transmission must also be considered [16].
• The Lord femoral component gave surprisingly good clinical long term results despite the bone remodeling (stress shielding), which in some cases was pronounced [17].

Anatomical context of C1QTNF5

• Interaction with CTRP5 was studied by immunoprecipitation and immunoblot analysis, using mouse eye and human retinal pigmented epithelium (RPE) choroid extracts and by expressing full-length CTRP5 and MFRP in a heterologous system [2].
• CONCLUSIONS: MFRP is localized to the plasma membrane of CE and RPE, and colocalizes and interacts with CTRP5 indicating a functional relationship between these two proteins [2].
• Anthony Eden's (Lord Avon) biliary tract saga [18].
• CONCLUSIONS: CTRP5, a secretory and membrane-associated protein, is localized to the lateral and apical membranes of the RPE and CB [14].
• Furthermore, cultured cells were used to show that the CTRP5 is a secretory protein and that its secretion is impaired by the S163R mutation [14].

Associations of C1QTNF5 with chemical compounds

• A Lord endoprosthesis was used in nine hips and a Biomet endoprosthesis in six [19].
• Menz HB, Latt MD, Tiedemann A, Mun San Kwan M, Lord SR. Reliability of the GAITRite walkway system for the quantification of temporo-spatial parameters of gait in young and older people. Gait & Posture 2004;20(1):20-25 [20].
• Entitled Truants--The Story of Some who Deserted Medicine Yet Triumphed, the book was written by Lord Moynihan based on the Linacre lecture he delivered in Cambridge in 1936, the year of his death [21].
• Persons accused of religious heresy, political offenses, or violating social-class distinctions also might be charged with sodomy, as illustrated by the cases of Lord Audley, Earl of Castlehaven and John Atherton, Bishop of Waterford and Lismore [22].
• "Lysine is the Lord", thought some scientists in regard to the group interacting with fluorescein isothiocyanate in ATP-binding sites of P-type ATPases but, is it not cysteine [23]?

Other interactions of C1QTNF5

• Spatial and Temporal Expression of MFRP and Its Interaction with CTRP5 [2].
• The differential expression levels of eight positional candidate genes, including inflammation-related THY1 and C1QTNF5, were also confirmed [24].

Analytical, diagnostic and therapeutic context of C1QTNF5

• CTRP5 expression was also evaluated by in situ hybridization [13].
• Mutations in candidate genes were screened by sequencing. mRNA expression of CTRP5 and MFRP, which are bicistronic genes, was studied by semiquantitative RT-PCR (qRT-PCR) in various human tissues [13].
• The membrane association of CTRP5 in the RPE and CE was further confirmed by immunoelectron microscopy [14].
• Cellular location of wild-type and mutant CTRP5 in MDCK and COS-7 cells was determined by immunofluorescence and immunoblot analysis [14].
• CTRP5 protein expression and distribution were studied by Western blot analysis, immunohistochemistry, and immunoelectron microscopy [14].

References